Inhaled nitric oxide (iNO) has been reported capable of selectively reducing elevated pulmonary artery pressure (PAP), regardless of whether the pulmonary hypertension was induced by hypoxia or sepsis. However iNO is relatively difficult to administer or monitor. We wondered whether NP, chemically related to NO but more stable in solution, would also selectively reduce elevated pulmonary artery pressure when administered via the more familiar modality of nebulization.

Methods: 6 piglets were anesthetized, and mechanically ventilated. Systemic blood pressure (BP), PAP, and cardiac output (CO) were monitored continuously. The effects of 15 minutes of Neb-NP (10 mg/ml, dissolved in 0.9% NaCl, flow 4 lpm) were assessed in each piglet in two different protocols: 1) Hypoxia-induced pulmonary hypertension(HIPH) induced by ΔFiO2 from 0.30 to 0.07 (ΔPaO2 from 149 to 29 mm Hg); and 2) GBS-induced pulmonary hypertension (GBS-IPH) induced by GBS infusion @ 4 × 107 orgs/kg-min.

Results: PAP rose from 15 to 32 torr during HIPH, and 17 to 42 torr during GBS-IPH (both p< 0.01). During HIPH, nebulized NP reduced PAP in each piglet (32 to 21 torr; p< 0.01) without significantly affecting BP(100 to 95 torr) or CO (643 to 591 mL/min). The mean reduction in HIPH was 64%(range 36 - 77%; p< 0.01). In contrast, during GBS-IPH nebulized NP reduced PAP significantly but less extensively (ΔPAP from 41 to 38 torr; p< 0.05). The mean reduction in GBS-IPH was 14% (range: 1 - 28%; p< 0.05; p< 0.01 vs HIPH). Neither BP nor CO was significantly affected by Neb-NP during GBS-IPH. In both protocols, the reduction in PAP began within 2 minutes of the onset of nebulized NP, and appeared to reach a plateau by 15 minutes. No tachyphylaxis was noted during either protocol.

Conclusions: 1) Neb-NP selectively reduced elevated PAP in both hypoxia- and GBS-induced pulmonary hypertension. 2) However, Neb-NP was much more effective in reducing PAP in non-septic piglets. 3) Nebulized NP may be clinically beneficial in contexts where inhaled NO is impractical -- however its potential clinical effectiveness may vary as a function of the underlying etiology of the pulmonary hypertension.